Responses of cerebral arterioles to activation of β-adrenergic receptors during diabetes mellitus

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Abstract

Background and Purpose Diabetes mellitus impairs reactivity of large peripheral arteries and arterioles to activation of β-adrenergic receptors. The goal of this study was to determine whether diabetes mellitus alters dilatation of cerebral arterioles to activation of β-adrenergic receptors. Methods In vivo diameter of pial arterioles was measured in nondiabetic and diabetic (streptozotocin 50 to 60 mg/kg IP) rats during superfusion with isoproterenol, forskolin, and nitroglycerin. In addition, we examined the contribution of nitric oxide or a nitric oxide-containing compound in dilatation of pial arterioles in response to the agonists. Results Dilatation of pial arterioles in response to isoproterenol was significantly less in diabetic compared with nondiabetic rats (3±2% versus 14±1%, respectively, for 1.0 μmol/L isoproterenol). In contrast, dilatation of pial arterioles in response to nitroglycerin and forskolin was similar in nondiabetic and diabetic rats. Furthermore, dilatation of pial arterioles in nondiabetic rats in response to isoproterenol and forskolin was not related to the synthesis and release of nitric oxide or a nitric oxide-containing compound. Conclusions The findings of the present studies suggest that diabetes mellitus impairs dilatation of cerebral resistance arterioles in response to activation of β-adrenergic receptors. Impairment of β-adrenergic-mediated dilatation of cerebral arterioles during diabetes mellitus does not appear to be related to an alteration in cyclic adenosine monophosphate, since forskolin produced similar vasodilatation in nondiabetic and diabetic rats.

Original languageEnglish (US)
Pages (from-to)141-145
Number of pages5
JournalStroke
Volume25
Issue number1
StatePublished - Jan 1 1994

Fingerprint

Arterioles
Adrenergic Receptors
Diabetes Mellitus
Dilatation
Colforsin
Isoproterenol
Nitric Oxide
Nitroglycerin
Streptozocin
Vasodilation
Cyclic AMP
Adrenergic Agents
Arteries

Keywords

  • Cerebral circulation
  • Diabetes mellitus
  • Rats
  • Vasodilation

ASJC Scopus subject areas

  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine
  • Advanced and Specialized Nursing

Cite this

Responses of cerebral arterioles to activation of β-adrenergic receptors during diabetes mellitus. / Mayhan, William.

In: Stroke, Vol. 25, No. 1, 01.01.1994, p. 141-145.

Research output: Contribution to journalArticle

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abstract = "Background and Purpose Diabetes mellitus impairs reactivity of large peripheral arteries and arterioles to activation of β-adrenergic receptors. The goal of this study was to determine whether diabetes mellitus alters dilatation of cerebral arterioles to activation of β-adrenergic receptors. Methods In vivo diameter of pial arterioles was measured in nondiabetic and diabetic (streptozotocin 50 to 60 mg/kg IP) rats during superfusion with isoproterenol, forskolin, and nitroglycerin. In addition, we examined the contribution of nitric oxide or a nitric oxide-containing compound in dilatation of pial arterioles in response to the agonists. Results Dilatation of pial arterioles in response to isoproterenol was significantly less in diabetic compared with nondiabetic rats (3±2{\%} versus 14±1{\%}, respectively, for 1.0 μmol/L isoproterenol). In contrast, dilatation of pial arterioles in response to nitroglycerin and forskolin was similar in nondiabetic and diabetic rats. Furthermore, dilatation of pial arterioles in nondiabetic rats in response to isoproterenol and forskolin was not related to the synthesis and release of nitric oxide or a nitric oxide-containing compound. Conclusions The findings of the present studies suggest that diabetes mellitus impairs dilatation of cerebral resistance arterioles in response to activation of β-adrenergic receptors. Impairment of β-adrenergic-mediated dilatation of cerebral arterioles during diabetes mellitus does not appear to be related to an alteration in cyclic adenosine monophosphate, since forskolin produced similar vasodilatation in nondiabetic and diabetic rats.",
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